NAJRAN UNIVERSITYCollege of Medicine

Microbiology &Immunology CourseLecture No. 20

By

Dr. Ahmed Morad AsaadAssociate Professor of Microbiology

Virus-cell interactionsReplication

Viruses multiply only in living cellsThe replication cycle consists of the following

steps:

1- Attachment (adsorption)•Viral replication starts with interaction of the virus with specific receptors on the cell surface•Receptor molecules differ for different viruses (viral tropism)•Antiviral antibodies can inhibit this process

2- Penetration (Engulfment)•Non-enveloped viruses penetrate the host cell by a process of phagocytosis forming a cytoplasmic vacuole that will dissolve releasing the nucleocapsid into the cytoplasm

•Enveloped viruses penetrate the cell by fusion of the viral envelope with the cell membrane releasing the nucleocapsid into the cytoplasm

3- Uncoating•It is the physical separation of viral nucleic acid from its capsid

4- Eclipse phase•During this period (some hours), several enzymes are produced by the host cells under control of viral genome•The cell metabolism is now directed to the synthesis of new viral particles•This phase ends with the formation of the infectious virus

5- Synthesis of viral components•Transcription of mRNA from viral nucleic acid•The virus utilizes cell components to translate mRNA into viral components

•In DNA viruses:•mRNA is transcribed by host cell DNA dependant RNA polymerase

•In RNA viruses:Viral RNA acts as a mRNA (+ve sense or +ve strand virus)Viral RNA should be transcribed to mRNA (-ve sense or –ve strand virus)

6- Assembly•Viral nucleic acid becomes surrounded by its capsid to form the mature virion (nucleocapsid)

7- Release•Release of viruses to extracellular environment either by cell lysis or by budding through cell membrane leaving the host cell intact•Enveloped viruses mature by a budding process

Inclusion bodies:•They are virus specific structures produced in the course of viral replication. (Areas of viral assembly)•Inclusion bodies may be:

Intranuclear: e.g. herpes virusesIntracytoplasmic: e.g. pox virusesIn both: e.g. measles virus

•Their presence in the cells is diagnostic of:Negri bodies in RabiesGuarnieri bodies in small poxTorr’s bodies in yellow fever

Pathogenesis of viral infections:The outcome of virus-cell interaction may be:•Cell death or lysis

•Abortive infection: No synthesis of new viral particles. Viral replication is blocked

•Latent infection: The viral genome persist inside the host cell for a period. There will be flare-up of clinical disease

•Transformation: The host cell will acquire new characters leading to rapid growth and malignancy

Viral infections may be:•Superficial: short incubation period – No invasion. E.g. Influenza viruses, Rota virus

•Systemic: After viral entry, it will spread to local lymphoid tissues followed by viraemia and spread to target organs.Examples:Skin & M.M. in measles and chicken poxLiver in hepatitis virusesMeninges in enterovirus meningitis

•Persistent: The virus will persist for a long period. Three types of persistent viral infections:

1- Chronic infection: leading to chronic diseases as in HBV and HCV

2- Latent infection: The virus persists silent for a period of time with intermittent flare-up. E.g., herpes

3- Slow virus infection: A very long incubation period, gradual onset and progressive course. E.g., AIDS